B6.129S7-Chrna7^tm1Bay/J

Stock number: 003232
Product name: Acrα7-
Research areas: Neurobiology Research

Description

These alpha7 nicotinic acetylcholine receptor knockout mice may be useful in studying the cholinergic anti-inflammatory pathway; including inflammatory neurotoxicity in stroke, myocardial infarction, sepsis and Alzheimer's disease, as well as neuropsychiatric diseases such as schizophrenia.

Detailed description

Mice homozygous for the alpha7 nicotinic acetylcholine receptor null allele (α7 nAChR- or α7-) are viable and fertile. Neuropathological and histochemical assessment of brains from α7 nAChR knockout mice reveal no abnormalities. High-affinity nicotine binding sites are present but there is an absence of high-affinity [I-125] alpha-bungarotoxin sites. Homozygotes lack rapidly desensitizing, methyllycaconitine-sensitive, nicotinic currents that are present in hippocampal neurons.

Development

A null mutation of the alpha7 subunit was prepared by deleting the last three exons (8-10) of the Chrna7 gene. Mice deficient in the alpha 7 subunit were generated by introducing a 7 kb deletion into ES cells. The strain originated on a mixed 129/SvEv and C57BL/6 background. The donating investigator backcrossed these mice to C57BL/6 for approximately eight generations ("N8F8") prior to sending to The Jackson Laboratory.

Allele

Symbol: Chrna7^tm1Bay
Name: targeted mutation 1, Baylor College of Medicine
MGI accession ID: MGI:1888407
Generation method: Targeted
Attributes: Null/Knockout
Marker symbol: Chrna7
Marker name: cholinergic receptor, nicotinic, alpha polypeptide 7
Chromosome: 7
Strain of origin: 129S7/SvEvBrd-Hprt1^b-m2
Molecular note: A 7 kb genomic fragment containing exons 8-10 was replaced with a neomycin selection cassette. The deleted sequences encode the second through the fourth transmembrane domains and the cytoplasmic loop. Northern blot analysis on brain samples derived from homozygous mice demonstrated that no detectable transcript was produced from this allele. Western blot analysis on brain extracts derived from homozygous mice also confirmed that no detectable protein was made from this allele.